Search Results (175)

Background: Postoperative pain management after a cesarean section remains a significant challenge, as inadequate control can delay maternal recovery and hinder early bonding and breastfeeding. While multimodal analgesia is the standard approach, non–pharmacological strategies like immediate skin–to–skin contact (SSC) are often underused despite their potential benefits in reducing pain, improving uterine contractions, and increasing maternal satisfaction. Objective: To evaluate the effects of immediate SSC on postoperative pain perception, uterine contraction quality, and maternal satisfaction, and to explore ways to incorporate SSC into routine post–cesarean care to promote recovery and humanized care. Method: A randomized clinical trial was conducted with 80 women undergoing elective cesarean sections, divided into two groups: SSC (40 women) and control (40 women). Postoperative pain was measured using the Visual Analog Scale (VAS) at various intervals, while uterine contraction quality and maternal satisfaction were assessed through clinical observation and a Likert scale, respectively. Results: We found that women in the SSC group experienced significantly lower pain scores (VAS2 and VAS3, p < 0.001), stronger infraumbilical uterine contractions (92.5%, p < 0.001), and higher satisfaction levels (average 9.98 vs. 6.50, p < 0.001). An inverse correlation was observed between pain intensity and satisfaction, indicating that SSC enhances both physiological and psychological recovery. Conclusions: Immediate SSC after cesarean is an effective, humanizing intervention that reduces pain, supports uterine contractions, and boosts maternal satisfaction. These findings advocate for integrating SSC into standard postoperative care, aligning with ethical principles of beneficence and autonomy. Further research with larger samples is necessary to confirm these benefits and facilitate widespread adoption in maternity protocols. Full article

Background/Objectives: Systemic sclerosis (SSc) is a multisystemic chronic autoimmune disease, which leads to disability and possibly early retirement. The objective of our study was to explore the associations between employment status (ES) and demographic, clinical and functional features in a single-center EUSTAR cohort. Methods: Consecutive patients with SSc examined between November 2011 and June 2023, who were under the age of retirement in our country (62 years for women, 65 for men at the time), were included. All patients underwent a comprehensive clinical assessment and filled in a work assessment questionnaire as well as two validated health-related questionnaires: the Scleroderma Health Assessment Questionnaire (SHAQ) and the Duruoz Hand Index (DHI). Associations between ES and potential predictors (education level, disease characteristics, work conditions, SHAQ and DHI) were tested using logistic regression adjusted for age and gender. Results: Ninety-one patients (mean ± SD age 53.7 ± 11.8 years, twenty-two with diffuse skin involvement, fifty-six with a history of digital of digital ulcers (DUs)), were included. Only 22 patients were still employed, while 69 were retired, of which 38 retired because of SSc. Among the employed, nine performed manual labor, nine spent many hours standing and three had to work in a cold environment. When potential predictors were tested separately, adjusted for age and sex, patients with higher education (OR (95% CI) 11.36 (2.03–63.36), p = 0.006) and no history of digital ulcers had higher odds of being employed. The presence of joint contractures and weightlifting as a work demand were associated with unemployment. In a multivariable model, higher education (OR 5.91, 95% CI 0.97–36.09, p = 0.054 and younger age (OR 0.90, 95% CI 0.85–0.96, p = 0.001) were independently associated with continued employment. High school education did not show a significant effect (OR 0.089, 95% CI 0.015–0.530, p = 0.008). Patients with a history of digital ulcers had the lowest employment rates compared to those with no digital ulcer history. No significant associations were found between employment status and SHAQ or DHI scores. Conclusions: SSc is associated with significant work disability and early retirement. Higher education, the lack of Dus and younger age were highly associated with staying employed. Given the rarity of SSc, we consider that our good sample size (n = 91) reflects disease prevalence, but results should be tested in other studies and the single center should be considered when interpreting generalizability. Full article

Pulmonary arterial hypertension (PAH) is a severe complication associated with connective tissue diseases (CTDs), which is characterized by a significant influence on the patient’s prognosis and mortality. The prevalence of PAH varies depending on the type of CTD. Still, it is highly prevalent in patients with systemic sclerosis (SSc), systemic lupus erythematosus (SLE), mixed connective tissue disease (MCTD), and primary Sjögren’s syndrome (pSS). Identifying rheumatic disease-specific risk factors is crucial for early diagnosis and intervention. Risk factors for PAH development include specific sociological factors (related to race, gender, and age), clinical features (particularly severe Raynaud’s phenomenon and multiple telangiectasias), cardiological factors (pericarditis and left heart disease), biochemical factors (elevated NT-proBNP and decreased HDL-cholesterol), serological factors (presence of ANA, e.g., anti-U1-RNP or SSA, and antiphospholipid antibodies), and pulmonary factors (interstitial lung disease and decreased DLCO or DLCO/alveolar volume ratio < 70%, FVC/DLCO > 1.6). The analysis of risk factors can be the most useful during the selection of patients at high risk of PAH development. The initial diagnosis of PAH is usually based on transthoracic echocardiography (TTE) and is finally confirmed by right heart catheterization (RHC). Targeted therapies can improve outcomes and include endothelin receptor antagonists, prostacyclin analogs, phosphodiesterase inhibitors, and tailored immunosuppressive treatments. Effective management strategies require a multidisciplinary approach involving rheumatologists, cardiologists, and pulmonologists. The risk stratification and individualized treatment strategies can enhance survival and quality of life in patients with PAH-CTD. Full article

Objectives: Systemic sclerosis-related interstitial lung disease (SSc-ILD) has high associated morbidity and mortality. With early diagnosis and treatment, we can improve clinical outcomes with immunosuppression. Some patients develop progressive pulmonary fibrosis (PPF) and are eligible for anti-fibrotic therapy. There are limited data on the incidence and prevalence of PPF in the SSc ILD cohort to guide case finding. We investigated this using data from UK tertiary Rheumatology and ILD centres. Methods: Patients with systemic sclerosis across two UK rheumatology units were identified using electronic records searched from 2021 to 2023 and were compared against established PPF diagnostic criteria. Results: 255 patients were identified. Prevalence of PPF was 5.49% and in those with established SSc-ILD, 23%. Median time to development of PPF was 5 years. In 64% of patients with PPF diagnosis, they had had systemic sclerosis for over 10 years. Incidence of PPF in patients with SSc was 3.9% and in those with known SSc-ILD 16.%. Only 50% of patients who met criteria for PPF had been referred to respiratory for consideration of antifibrotic initiation. Patients with a predominantly fibrotic baseline radiological pattern (UIP) had a trend towards development of PPF (p = 0.07). No patient with a predominantly inflammatory baseline pattern developed PPF (p = 0.021). Conclusions: Real world data have shown a prevalence of PPF in the SSc-ILD cohort of 23% with a median time of 5 years to development from diagnosis of SSc. Our data show active case finding may be incomplete and rheumatologists must be cognisant of PPF when evaluating patients with SSc. Full article

Systemic sclerosis (SSc) is an autoimmune fibrotic disorder affecting the skin and internal organs, categorized as either limited cutaneous SSc, where distal areas of skin are involved, or diffuse cutaneous SSc, where more extensive proximal skin involvement is seen. Vascular remodelling and internal organ involvement are frequent complications in both subsets. Multiple pathogenic mechanisms have been demonstrated, including production of disease-specific autoantibodies, endothelial cell damage at an early stage, infiltration of involved tissues by immune cells, as well as environmental factors triggering the onset such as solvents and viruses. Although not strongly familial, susceptibility to SSc is associated with multiple single nucleotide polymorphisms in immunoregulatory genes relevant to antigen presentation, T cell signalling and adaptive immunity, as well as innate immunity. In addition, several lines of evidence demonstrate abnormalities within the epithelial cell layer in SSc. Macroscopically, the SSc epidermis is pigmented, thickened and stiff and strongly promotes myofibroblasts in co-culture. Moreover, multiple activating factors and pathways have been implicated in the disease epidermis, including wound healing responses, induction of damage associated molecular patterns (DAMPS) and the release of pro-fibrotic growth factors and cytokines. Similar to SSc, data from studies of cutaneous wound healing indicate a major role for epidermal keratinocytes in regulating local fibroblast responses during repair of the wound defect. Since the epithelium is strongly exposed to environmental factors and richly populated with protective immune cells, it is possible that disease-initiating mechanisms in SSc involve dysregulated immunity and tissue repair within this cell layer. Treatments designed to restore epithelial homeostasis or else disrupt epithelial–fibroblast cross-talk could be of benefit in this severe and resistant disease. Accordingly, single cell analysis has confirmed an active signature in SSc keratinocytes, which was partially reversed following a period of JAK inhibitor therapy. Full article

Objective: The development of a normal sleep–wake rhythm in the first weeks of life depends on the physiological sensory needs of the newborn as well as the environment surrounding them. This includes, for example, avoiding pain, exposure to bright light at night and high noise levels. In high-risk newborns, this process can be influenced by immaturity of the central and peripheral nervous systems, therapeutic strategies and the work organization of an intensive care unit. Methods: This study used a narrative review to examine the literature on the interrelationship of sensory modalities on sleep–wake behavior in the context of neonatal intensive care. The current Cochrane reviews on cycled lighting’s effect on premature infants’ circadian rhythm development and noise or sound management in the neonatal intensive care unit, as well as the World Health Organization (WHO) global position paper on kangaroo mother care, were included. Results: An extensive body of literature relates to fetal and neonatal development of the five sensory modalities: touch, taste, smell, hearing and sight. In contrast, there is a lack of evidence regarding the choice of optimal lighting and suitable measures for noise reduction. Since 2023, the WHO has recommended that, from the moment of birth, every “small and sick” newborn should remain in skin-to-skin contact (SSC) with their mother. Developmental support pursues a multimodal approach with the goal of fostering early parent–child bonding, including the child’s needs and environmental conditions. Discussion: The implementation of early SSC and attention to the sleep–wake cycle require systemic changes in both the obstetric and neonatal settings to ensure seamless perinatal management and subsequent neonatal intensive care. Since there is a lack of evidence on the optimal sensory environment, well-designed, well-conducted and fully reported randomized controlled trials are needed that analyze short-term effects and long-term neurodevelopmental outcomes. Full article

Background/Objectives: Systemic sclerosis (SSc) is a progressive autoimmune disease characterized by widespread fibrosis, including skin thickening. Mycophenolate mofetil (MMF) is commonly used in SSc-associated interstitial lung disease, but its efficacy in improving skin fibrosis has not been systematically evaluated. This study aimed to assess the therapeutic effect of MMF on cutaneous sclerosis in SSc, as measured by the modified Rodnan skin score (mRSS). Methods: A systematic review and meta-analysis were conducted following PRISMA 2020 guidelines. PubMed, Embase, and Web of Science were searched from January 2000 to March 2025. Studies reporting mRSS outcomes in SSc patients treated with MMF were included, provided that the effect of MMF could be separately evaluated when used alongside other therapies. Risk of bias was assessed using the Cochrane RoB 2.0 tool for randomized controlled trials and the ROBINS-I tool for non-randomized studies. A random-effects model was used to estimate the pooled mean change in mRSS. Heterogeneity and publication bias were evaluated. Results: Eight studies involving 569 patients were included. The pooled mean reduction in mRSS following MMF treatment was −5.82 (95% CI: −7.46 to −4.19), exceeding the minimal clinically important difference. Heterogeneity across studies was substantial (I² = 82.6%). A post hoc exploratory subgroup analysis suggested greater improvement in early disease (<2 years), though this finding requires confirmation in prospective studies. MMF was generally well tolerated, with low discontinuation rates due to adverse events. Conclusions: MMF is associated with a statistically and clinically significant improvement in skin fibrosis in patients with SSc. These findings support its use as a frontline therapy for progressive cutaneous involvement, although further prospective studies are needed to identify optimal candidates for treatment. Full article

The mortality risk in systemic sclerosis (SSc) is primarily determined by pulmonary involvement (interstitial lung disease (ILD), pulmonary fibrosis), pulmonary arterial hypertension (PAH), and cardiac involvement. With timely and intensive treatment, the disease can be halted or even improved. Therefore, early diagnosis remains crucial. Unfortunately, biomarkers currently available cannot meet this requirement. SSc is characterized by autoimmune inflammation, vasculopathy, and fibrosis. The immunometabolic characterization of autoimmune diseases contributes to a better understanding of the underlying inflammatory processes. In this narrative review, we included 13 studies on metabolomic patterns in SSc in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses Guidelines (PRISMA). Current studies indicate an altered metabolome in SSc. All documented significant differences between patients with SSc and healthy controls, although the observed metabolomic patterns in SSc were inconsistent between studies. Metabolome alterations include, in particular, energy-related metabolic pathways such as glycolysis/gluconeogenesis, including the synthesis and degradation of ketones, fatty acid oxidation, amino acid-related metabolic pathways, lipid metabolism, and the tricarboxylic acid (TCA) cycle, including pyruvate metabolism. The most frequently examined organ complications with reported significant aberrations of the metabolome were skin involvement, ILD, and PAH. Conclusion: The detailed characterization of the SSc-specific metabolome promises a more comprehensive understanding of the pathogenic mechanisms of the disease. Furthermore, the detection of associations between specific metabolic aberrations and disease phenotypes bears hope for new biomarkers and an improved personalized approach to diagnostics, therapy, and follow-up in the management of SSc. Full article

Background: Systemic sclerosis (SSc) is a rare connective tissue disease characterized by vasculopathy, autoimmunity, and fibrosis. Due to its low prevalence and heterogeneous clinical presentation, early diagnosis remains challenging, often delaying appropriate treatment. The disease progresses from microvascular dysfunction, manifesting as Raynaud’s phenomenon, to systemic fibrosis affecting multiple organs, including the lungs, gastrointestinal tract, heart, and kidneys. There have been considerable advancements in understanding the pathophysiology of the disease during the last few years and this has already resulted in the improvement of the therapeutic approaches used to control organ-specific manifestations. However, the underlying cause of the disease still remains incompletely elucidated. Methods: Here, we summarize the current knowledge on the SSc pathogenesis. Results: The pathophysiology involves an interplay of chronic inflammation, impaired vascular function, and excessive extracellular matrix deposition, leading to progressive organ damage. Endothelial dysfunction in SSc is driven by immune-mediated injury, oxidative stress, and the imbalance of vasoconstrictors and vasodilators, leading to capillary loss and chronic hypoxia. Autoantibodies against endothelial cells or other toxic factors induce apoptosis and impair angiogenesis, further exacerbating vascular damage. Despite increased angiogenic factor levels, capillary repair mechanisms are defective, resulting in progressive ischemic damage. Dysregulated immune responses involving Th2 cytokines, B cells, and macrophages contribute to fibroblast activation and excessive collagen deposition. Transforming growth factor-beta (TGF-β) plays a central role in fibrotic progression, while fibroblasts resist apoptosis, perpetuating tissue scarring. The extracellular matrix in SSc is abnormally stiff, reinforcing fibroblast activation and creating a self-perpetuating fibrotic cycle. Conclusions: Advances in molecular and cellular understanding have facilitated targeted therapies, yet effective disease-modifying treatments remain limited. Future research should focus on precision medicine approaches, integrating biomarkers and novel therapeutics to improve patient outcomes. Full article

Systemic sclerosis (SSc) is a rare autoimmune connective tissue disease characterized by a widespread accumulation of extracellular matrix components leading to fibrosis of the skin and internal organs. Vascular changes occur in all involved tissues and are responsible for several distinctive clinical manifestations of the disease. This review focuses on the usefulness of various diagnostic tools in clinical practice for the early identification of clinical, functional, and/or structural RV impairment in SSc patients at risk of PH. It aims to identify specific causes of RV dysfunction, describe potential differences in outcome measures, and, ultimately, determine different cut-off values compared to subjects with PH not related to SSc. Full article

Systemic sclerosis (SSc) is a complex autoimmune disease characterized by vasculopathy, immune dysregulation, and progressive fibrosis affecting the skin and internal organs. Pulmonary complications, including interstitial lung disease (ILD) and pulmonary arterial hypertension (PAH), are major contributors to morbidity and mortality, while skin fibrosis remains a hallmark of disease heterogeneity. Despite advances in understanding SSc pathogenesis, early diagnosis and timely therapeutic intervention remain challenging due to the rapid progression of inflammation and the narrow window before irreversible fibrosis occurs. The identification of reliable biomarkers is crucial for improving diagnosis, monitoring disease activity, and guiding treatment decisions in SSc. While autoantibodies are well-established diagnostic tools, this review focused on non-autoantibody biomarkers, including soluble proteins, cytokines, chemokines, epigenetic modifiers, and oxidative stress indicators. These biomarkers reflect diverse pathogenic mechanisms such as endothelial injury, fibroblast activation, immune signaling, and extracellular matrix remodeling. By examining the available evidence across both clinical and preclinical studies, this review provides an updated overview of molecular markers involved in inflammation and fibrosis in SSc. Understanding their biological significance and therapeutic potential may improve risk stratification, guide targeted interventions, and ultimately contribute to the development of precision medicine strategies in systemic sclerosis. Full article

Background/Objectives: Rapid skin thickness progression assessed using the modified Rodnan skin score (mRSS) is associated with poor outcomes in systemic sclerosis (SSc). However, the correlation between patterns of skin thickness and the onset of internal organ involvement remains unclear. This study aimed to determine the correlation between peak skin thickness progression rate (pSTPR) and the onset of internal organ involvement, particularly interstitial lung disease (ILD) and pulmonary arterial hypertension (PAH) among Thai SSc patients. Method: A prospective cohort study with retrospective analysis was conducted on adult SSc patients who experienced the onset of their first non-Raynaud phenomenon symptoms between January 2013 and December 2020 and had at least a 2-year follow-up. Patients with an overlap syndrome were excluded from this study. The pSTPR was calculated by dividing the peak of the mRSS by the duration of disease at the peak of the mRSS. Result: A total of 509 patients were included in this study. The majority of cases were female (351; 69.0%) and comprised diffuse cutaneous SSc subsets (353 cases; 69.4%). The respective mean age and median pSTPR was 48.2 ± 11.6 years and 1.63 points/year (interquartile range 0.5–4.4). The respective median durations of disease at the onset of significant ILD (>20% extent), ILD, and mean duration of disease at the onset of PAH were 3.4 (Q1–Q3 1.4–7.7), 5.4 (Q1–Q3 2.4–9.2), and 8.0 ± 4.9 years. pSTPR was negatively correlated with disease duration at the onset of significant ILD (Rho −0.509, p < 0.001), ILD (Rho −0.480, p < 0.001), PAH (Rho −0.372, p = 0.03), and disease duration from onset to death (Rho −0.367, p = 0.03) after adjusting for age, sex, and anti-topoisomerase I. Conclusion: SSc patients with a high skin thickness progression rate reaching the maximum point of mRSS were at risk of developing early ILD, PAH, and death. The pSTPR may be used to assess individuals at risk of experiencing early onset cardiopulmonary involvement in SSc. Full article

Systemic sclerosis (SSc) is a complex autoimmune disease characterized by vasculopathy and tissue fibrosis affecting the skin and internal organs. Genetic and environmental factors influence susceptibility, severity, and onset. Current treatments are limited and not always effective, leading researchers to investigate new approaches, such as the use of adipose-derived mesenchymal stem cells (ADSCs) through fat grafting. This review seeks to understand how ADSCs may impact the development and progression of SSc, with a particular focus on how these cells could alter immune responses and reduce fibrosis. ADSCs have been found to affect various immune cells, including T cells, B cells, macrophages, and dendritic cells, by releasing cytokines, chemokines, and growth factors. These interactions generally suppress inflammation and promote a regulatory immune environment. Additionally, ADSCs can influence the extracellular matrix, helping to prevent fibrosis through signaling molecules like exosomes. ADSCs show promise as a treatment for SSc due to their ability to modulate the immune system and reduce fibrosis. Early clinical studies are encouraging, but more research is needed to fully understand how they work and to develop effective treatment protocols. Full article

Lung cancer remains the most common cancer worldwide, with a limited prognosis despite personalized treatment regimens. Low-dose computed tomography (CT) scanning as a means of early diagnosis has been disappointing due to the high false positive rate. Other non-invasive means of testing need to be developed that offer both timely diagnosis and predict prognosis. Methods: In the course of stool testing in large-scale testing of 2922 patients at increased risk of CRC, we were able to ascertain 112 patients documented to have prospectively been diagnosed with lung cancer. Stool and colonic effluents were tested for p87 with anti-adenoma antibody (Adnab-9) reactivity by ELISA and Western blot. Survival data were obtained where available. Results: Of 112 cancers, approximately 27.6% were squamous (SSC), 17.9% were adenocarcinoma, 8% were small, 6.25% were large cell, 3.57% were designated non-small cell cancer (NSCLC), 0.89% were indeterminate, 0.89% were lepidic spread, 3.57% had metastasis, and in 31.25%, data were unavailable. In total, 49.1% of the lung cancer patients had fecal Adnab-9 testing. Overall, 60% had positive testing compared to 38%, which was significant (OR2.19 [1.06–4.53]; p = 0.045). Cancers with higher lethality were less likely to test positive (approximately 8.5% each for both small and large cell lung cancers) and higher, with 56% for SCC and 25% for adenocarcinoma (0% NSCLC). In the larger groups, overall survival was worse in those testing positive: 474 testing positives versus 844 days in SCC and 54 testing positive versus 749 days in adenocarcinoma patients. Most importantly, the time from a positive test to the clinical diagnosis ranged from 2.72 years for small cell, 3.13 for adenocarcinoma, 5.07 for NSCLC, 6.07 for SSC, and 6.24 for large cell cancer. In excluded cases where cancer in the lung was believed to be metastatic, 83.3% of cancers were positive. Conclusions: At a projected real-world sensitivity of 0.60 and specificity of 0.60, and the ability to predate diagnosis by up to 4.7 years overall, this test could help direct lung cancer screening. In addition, the Adnab-9 testing selectively detects worse tumor types (87.5%) and those with worse prognoses amongst the more common, favorable phenotypes, thus making early diagnosis possible in those patients who stand to benefit most from this strategy. Metastatic lung cancer, also detected by the test, should be identified by the follow-up imaging studies and, therefore, would not be considered to be a major pitfall. Full article

Supersulfate cement (SSC) has received significant attention in the construction industry due to its extensive utilization of solid wastes and low carbon emissions. However, the low carbonation resistance and early strength of SSC greatly restricted its application, which was attributed to early insufficient alkalinity and slow hydration. Facilitating early hydration alkalinity is critical to promote early hydration and improve early performance for SSC. Thus, sodium aluminate (SA), an admixture with concentrations ranging from 0% to 4%, was adopted to enhance early alkalinity and investigate its impact on the initial hydration process. The results indicated that incorporating SA into SSC enhances its early performance by balancing high alkalinity and AFt stability. The addition of 2% SA accelerates hydration procession, reducing initial and final setting times by 76% and 42%, respectively, while increasing viscosity by 50% for improved structural stability. At 2% SA, 1-day and 7-day compressive strengths rose from 3.7 MPa to 8.4 MPa and from 15.1 MPa to 18.5 MPa, respectively, representing gains of 127% and 22.5%, which were facilitated by accelerated GGBFS dissolution and needle-like AFt formation, which densifies the crystal-gel network microstructure. Full article